Figure 2.

The effect of VPDs.

VPDs and infections can ultimately result in cardiovascular events.^34,42-46 Infection with pathogens associated with influenza-like illness leads to an increased pro-inflammatory response that exacerbates plaque formation in the blood vessels and procoagulant effects, which then contributes to accelerated atherosclerosis.³⁴ Influenza has also been shown to lower the anti-inflammatory properties of HDL cholesterol particles, which further drives the infiltration of macrophages through the arterial wall.⁴³ In addition, there is some evidence that influenza may increase the risk of tachycardia, which is associated with major adverse cardiovascular events in hypertensive patients.^43,45 Other viral infections may have similar outcomes: for example, the varicella zoster virus has been shown to directly cause pathologic vascular remodeling, resulting in a thickened intima and vascular occlusion, leading to subsequent thrombosis and rupture.^44,46 Varicella zoster virus also induces systemic inflammatory responses, which cause disruption to pre-existing atherosclerotic plaques and stimulate mediators of the coagulation system.^42,46 Altogether, these events increase the risk of stroke.^42,44,46

HDL, high-density lipoprotein; MI, myocardial infarction; VPD, vaccine-preventable disease.